Effects of Valsartan on Angiotensin II-Induced Migration of Human Coronary Artery Smooth Muscle Cells.

Abstract

The migration as well as proliferation of coronary artery medial smooth muscle cells (SMC) into the intima is proposed to be an important process of intimal thickening in coronary atherosclerosis.In the current study, we examined the effects of the angiotensin type 1 receptor antagonist valsartan on angiotensin II (Ang II)-induced migration of cultured human coronary artery SMC using Boyden's chamber methods. Ang II significantly stimulated human coronary artery SMC migration in a concentration-dependent manner between 10_6 and 10_8 mol/I when cells of passage 4 to 6 were used. However, the migration response to

Inhibition of Migration and Proliferation of Rat Vascular Smooth Muscle Cells by a New HMG-CoA Reductase Inhibitor, Pitavastatin

“…In the present study, we have confirmed our previous findings that Ang II and PDGF BB induced rat or human vascular SMC migration (14)(15)(16)21). We have also shown that a new HMG-Co A reductase inhibitor, pitavastatin, clearly suppressed Ang II-and PDGF BB-induced SMC migration at reported therapeutic concentrations (10 9 mol/l) (27).…”

“…Previously, we have shown that angiotensin II (Ang II) and platelet-derived growth factor (PDGF) stimulate migration and proliferation of SMCs via Ang II type 1 (AT1) receptors and PDGF β receptors, respectively (14)(15)(16). In particular, the importance of the renin-angiotensin system in SMCs proliferation and migration has been established in intimal lesion formations after balloon injury (17)(18)(19)(20)(21)(22)(23).…”

Effects of Angiotensin II Type 1 Receptor Antagonist on Smooth Muscle Cell Phenotype in Intramyocardial Arteries from Spontaneously Hypertensive Rats

“…First, the different effects on the phenotypic change of VSMCs in the intramyocardial arteries could be related to differences in the direct inhibition of Ang II stimulation through the AT1 receptor by FK-739 and enalapril, because it has been reported that Ang II might play an important role in the SMC phenotype change in SHR, but not WKY (9,13,(18)(19)(20), which is mainly controlled through the AT1 receptors (5,21), and an AT1 receptor antagonist has been shown to inhibit the Ang II-induced migration of coronary artery SMCs (22). In addition, the difference in the amount of stimulation through the Ang II type 2 (AT2) receptor may have contributed to the different results between FK-739 and enalapril (5).…”

Carvedilol Inhibits Pressure-Induced Increase in Oxidative Stress in Coronary Smooth Muscle Cells.

“…Human coronary artery SMCs were cultured in SmBM as previously reported (10). To avoid the differences in oxidative stress due to differences in number of cell passages, the experiments in the same figure or table were performed in the same passage.…”